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Query: UMLS:C0729233 (Thoracic)
 6,478 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diffuse interstitial lung disease in asbestos-exposed workers is presumed to represent asbestosis. Among 176 asbestos-exposed persons for whom lung tissue was available, we found nine with clinical features consistent with asbestosis, but histologic sections failed to demonstrate asbestos bodies, the usual requirement for pathologic diagnosis of asbestosis (Group I). These nine were compared by analytic electron microscopy with nine persons with idiopathic pulmonary fibrosis (Group II), and with nine persons with all the criteria of asbestosis (Group III). The three groups did not differ significantly with respect to lung burden of chrysotile or tremolite and actinolite, but Group III had a lung burden of amosite and crocidolite that was three orders of magnitude greater than in Groups I and II, with no overlap. We conclude that (1) the American Thoracic Society criterion of "a reliable history of exposure" is sometimes difficult to define; (2) asbestos bodies are seen in tissue sections only when exposure has been reasonably high, and given the proper clinical setting, the presence of diffuse fibrosis and asbestos bodies in tissue sections are sensitive and specific criteria for a diagnosis of asbestosis; and (3) the prevalence here of 5.1% nonasbestos-induced interstitial lung disease among asbestos-exposed persons is artefactually high because of atypical case selection. However, because asbestosis is a disappearing disease, such cases will become more frequent. The identification of these other diseases is important because therapy and prognosis may differ from that of asbestosis.
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PMID:Idiopathic pulmonary fibrosis in asbestos-exposed workers. 189 81

Usual interstitial pneumonitis (UIP) is a chronic pulmonary process with a characteristic peripheral fibrotic pattern on gross pathologic lung sections and CT scans. This condition is often idiopathic, but asbestosis, rheumatoid arthritis, and scleroderma may cause the same peripheral fibrosis in the lungs. UIP is associated with an increased incidence of pulmonary neoplasms. The purpose of this study was to evaluate the size of mediastinal lymph nodes in patients with UIP in whom no evidence was seen of malignancy or current active infection. CT scans of 14 patients (12 with idiopathic pulmonary fibrosis and two with collagen vascular disorders) were assessed for lymph node location (American Thoracic Society mediastinal map) and size. In 13 of 14 patients, nodes measured greater than threshold size values. Nodes as large as 20 x 30 mm were identified in three patients. Nodal sites 10R, 4R, 2R, 5, and 6 were most commonly abnormal. We conclude that increase in the size of mediastinal lymph nodes as shown on chest CT scans is common in patients with UIP, occurs without superimposed infectious or malignant complications, and is thus presumably part of the chronic inflammatory process. Consequently, lymphadenopathy in these patients does not suggest that they have lung cancer also.
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PMID:Mediastinal lymph node enlargement on CT scans in patients with usual interstitial pneumonitis. 210 8

Simple tests of lung function may be misleading in the assessment of patients with interstitial lung disease. Eight patients are described with cryptogenic fibrosing alveolitis (histologically proven in four) with severe breathlessness and low gas transfer (median DLCO 32.4%, range 9.2 to 35.3%, % predicted) in whom lung volumes were preserved [median VC 98.7, range 67.5-131.1%; median TLC 92.5, range 88.1 to 121.2, (% predicted)], and in whom there was no evidence of airflow obstruction [median FEV1/FVC 84.6, range 68-116 (% predicted)]. All were current or ex-heavy smokers. Thoracic high resolution computed tomography revealed upper zone emphysema, the extent of which was not appreciated using conventional chest radiography. The atypical physiological and radiological features can be explained by coincidental cryptogenic fibrosing alveolitis and emphysema and high resolution computed tomography was valuable in the assessment of these patients.
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PMID:Combined cryptogenic fibrosing alveolitis and emphysema: the value of high resolution computed tomography in assessment. 224 66

A case of advanced cryptogenic fibrosing alveolitis (CFA) with multiple bullae and extensive pulmonary fibrosis, scheduled for modified radical mastectomy for carcinoma of breast, is presented. This patient had ischemic heart disease, corticosteroid-induced hypertension, diabetes mellitus, and a difficult airway. Thoracic epidural segmental anesthesia was successfully given to this patient. Preoperative problems, perioperative management, and alternative anesthetic techniques are discussed.
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PMID:Thoracic epidural anesthesia for modified radical mastectomy in a patient with cryptogenic fibrosing alveolitis: a case report. 1077 15

Over the last 30 years the clinical and histopathological definitions of the diffuse lung diseases have evolved considerably. Initially pathological entities were defined in parallel with clinico-radiological diagnoses, but these have more recently become consolidated into a more meaningful combined classification. These refinements have impacted on the diffuse lung diseases in particular, and have defined individual diseases more precisely than in previous classifications in which a number of distinct entities had been grouped together and mistaken for idiopathic pulmonary fibrosis, resulting in much confusion. The American Thoracic and European Respiratory Societies' committees, charged with the task of defining the idiopathic interstitial pneumonias, have recently published a statement on idiopathic pulmonary fibrosis, and a statement on the other idiopathic interstitial pneumonias should follow this year. Of these diseases, idiopathic pulmonary fibrosis is the most lethal, and this review deals with the impact that the changes in the nomenclature will have on our understanding of this and the other diseases with which idiopathic pulmonary fibrosis was previously confused and explores the implications of our new understanding on clinical practice. It also attempts to highlight areas of previous dogma in the literature that now need to be re-considered in the context of these more recent statements.
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PMID:Idiopathic interstitial pneumonias: a re-appraisal of idiopathic pulmonary fibrosis. 1176 66

Understanding of the cellular and cytokine interactions associated with inflammation and fibrosis in interstitial lung diseases (ILDs) has increased substantially during the past few years. Presently, many agents are known to have the ability to induce ILDs, although only a small percentage of exposed individuals will develop the disease. In addition, the majority of ILDs are of unknown origin and many are labelled "idiopathic". Therefore, host susceptibility, genetic factors and, possibly, environmental cofactors may be important for the clinical expression of ILDs. The present review reports evidence of the genetic predisposition to develop ILDs of unknown origin, more specifically sarcoidosis, idiopathic pulmonary fibrosis (IPF), lymphangioleio-myomatosis and ILDs, in systemic sclerosis. For instance, for sarcoidosis and IPF several histocompatibility antigens have been associated with the development and/or the clinical presentation of the disease. Furthermore, there are also several types of ILD that are associated with inherited disorders, of which the tuberous sclerosis complex is only one example. This clearly indicates that pulmonary fibrosis can be influenced by genetic factors. Familial occurrence of sarcoidosis and IPF is also well known, although the exact modes of inheritance are debatable. Several studies have shown that extrinsic factors, such as single or multiple fibrosing agents, probably contribute to the development of clinical ILDs of unknown origin. It is probable that some of these studies deal with patients who do not have classical IPF, as recently defined by the American Thoracic Society (ATS)/European Respiratory Society (ERS) consensus. Therefore, the true role of these extrinsic factors in the development of IPF, or even sarcoidosis, remains speculative. With the help of animal studies and, more specifically, by using knock-out mice, it may be possible in the near future to unravel at least some of the genes that are responsible for the increased susceptibility of the development of interstitial lung diseases.
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PMID:Genetic predisposition and pathogenetic mechanisms of interstitial lung diseases of unknown origin. 1181 21

A 9-year-old, spayed, female West Highland white terrier was presented with a chronic cough, lethargy, and exercise intolerance. Thoracic radiographic findings were consistent with a marked interstitial lung pattern. Idiopathic pulmonary fibrosis, a disease anecdotally linked to this breed, was diagnosed on postmortem examination.
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PMID:Chronic idiopathic pulmonary fibrosis in a West Highland white terrier. 1224 May 28

Idiopathic pulmonary fibrosis (IPF) is defined as a specific form of chronic fibrosing interstitial pneumonia limited to the lung and associated with the histologic appearance of usual interstitial pneumonia (UIP) on lung biopsy. It is characterized by progresive dyspnea, worsening of pulmonary function and radiographically, by patchy subpleural interstitial infiltrates with minimal ground glass appearance predominantly affecting the lung bases. The etiology is unknown and no therapy has been clearly shown to prolong survival. The diagnosis, which earlier was difficult to establish, is now based on guidelines of American Thoracic Society. Newer insight into its etiopathogenesis, particularly the mechanisms involved including T helper 1 (Th1) and T helper 2 (Th2) types of responses occurring after the initial and repetitive lung insults and the ineffectiveness of conventional modes of therapy has prompted clinicians worldwide to look for alternative modes of therapy. Conventional therapy for this disorder has been steroids and immunosuppressives. Immunomodulators (Interferon gamma 1b) and antioxidants (Glutathione and its precursor N-acetyl cysteine) are promising results in this, otherwise, uniformly fatal condition.
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PMID:Idiopathic pulmonary fibrosis: newer concepts and management strategies. 1268 10

The American Thoracic Society and the European Respiratory Society 2002 classification defines the histologic patterns that provide the basis for a clinico-radiologic-pathologic diagnosis of an idiopathic interstitial pneumonia. Idiopathic pulmonary fibrosis is the clinical term for usual interstitial pneumonia, the characteristic histologic pattern is interstitial fibrosis with temporal heterogeneity, and the radiologic pattern is basal and subpleural areas of ground-glass and reticular attenuation and honeycomb pattern. Nonspecific interstitial pneumonia has cellular or fibrosing patterns of chronic inflammation with temporal homogeneity; the radiologic pattern is subpleural and basal areas of ground-glass and reticular attenuation. Lymphoid interstitial pneumonia results from lymphocyte interstitial infiltration; CT demonstrates ground-glass attenuation and nodular interlobular septal thickening. Respiratory bronchiolitis-associated interstitial lung disease is characterized by bronchiolocentric alveolar macrophage accumulation; CT shows centrilobular ground-glass attenuation. Desquamative interstitial pneumonia is characterized by alveolar macrophage accumulation with predominantly lower zone ground-glass attenuation seen on CT scans. Cryptogenic organizing pneumonia is characterized radiologically by peribronchial ground-glass attenuation and subpleural consolidation. Acute interstitial pneumonia is the clinical term for idiopathic diffuse alveolar damage; the exudative phase is characterized radiologically by diffuse ground-glass attenuation and dependent consolidation, with the additional feature of lung architectural distortion in the organizing phase. Ideally, diagnosis of an idiopathic interstitial pneumonia should be rendered only after all clinico-radiologic-pathologic data have been reviewed.
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PMID:CT-histologic correlation of the ATS/ERS 2002 classification of idiopathic interstitial pneumonias. 1297

Idiopathic pulmonary fibrosis (IPF), synonymous with cryptogenic fibrosing alveolitis (CFA), is a progressive and usually fatal disease of unknown cause characterized by sequential acute lung injury with subsequent scarring and end-stage lung disease. Historically, IPF/CFA encompassed a heterogeneous group of different histological and clinical entities arising in an idiopathic setting. Recently, the American Thoracic Society (ATS) and European Respiratory Society (ERS) core committee has redefined diagnostic criteria for both IPF/CFAand idiopathic interstitial pneumonias confining the term IPF/CFA to patients with a histological pattern of usual interstitial pneumonia on lung biopsy. This review attempts to refine the clinico-radiological-pathological features that together define IPF/CFA as it is understood today, and to summarize the rationale of new therapeutic approaches based on the current understanding of the pathogenetic mechanisms.
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PMID:Idiopathic pulmonary fibrosis/cryptogenic fibrosing alveolitis. 1459 83


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